Blowfly flight muscle mitochondria undergo a dramatic decline in their capacity to carry out respiration-linked calcium transport as the flight muscle undergoes the transition from development to maturity and senescence. The mitochondria also undergo changes in their membrane structure that make them more permeable to some anions in the sensescent compared to the mature flight muscle tissue. The primary objective of this research proposal is to throughly characterize the decline in calcium transport capacity to understand better: (1) the mechanism of respiration-linked calcium transport and (2) the role of calcium in developing and aging muscle tissue. The investigation into these two aspects will also involve the identification of (1) the modifications in the anion transport capacity (phosphate, pyruvate, and adenine nucleotides) and (2) the biochemical controls that may be responsible for the termination of the biosynthetic capacity of the flight muscle mitochondria during old age. It is hoped that these investigations can be extended to the mitochondria from tissue-cultured skeletal muscle cells that undergo terminal differentiation and where the transitions in mitochondrial biosynthetic capacity can be investigated.